ACUTE KIDNEY INJURY

AND CHRONIC KIDNEY

DISEASE

Dr, Rusdiana, M.Sc.,SpPD

Penyakit Dalam RS Prasetya Bunda
Tasikmalaya
Outline
Epidemiology
Anatomy & Physiology
AKI vs ARF
CKD
Dyalisis
 Anatomy & Physiology
The Urinary
System
Female
Male

Urology &
Nephrology
The
Kidneys
 Anatomy & Physiology
The
Kidneys
Hilum
Medulla
Pyramids
Papilla
Renal Pelvis
ARF vs AKI
AKI Definition
AKI is dened as any of the following :
- increase in SCr by >0.3 mg/dl
(>26.5lmol/l) within 48 hours; or
-Increase in SCr to>1.5 times baseline,
which is known or presumed to have
occurred within the prior 7 days; or
-Urine volume <0.5 ml/kg/h for 6 hours.
Stage of AKI:

Stage 1 1.5-1.9 times baseline OR

0.3 mg/dl (26.5 micromol/l) increase in the serum
creatinine, OR urine output <0.5 ml/kg per hour for 6
to 12 hours.
Stage 2 2.0-2.9 times baseline increase in the
serum creatinine OR urine output <0.5 ml/kg per
hour for 12 hours.
Stage 3 3.0 times baseline increase in the serum
creatinine OR increase in serum creatinine to
4.0mg/dl (353.6 micromol/l) OR urine output of
<0.3 ml/kg per hour for 24 hours, OR anuria for
12 hours OR the initiation of renal replacement
therapy OR, in patients <18 years, decrease in
estimated GFR to <35 ml/min per 1.73m2
types of acute kidney injury
 I. Pre-renal injury

In pre-renal failure, the renal tissue is intact and kidney

biopsy shows normal renal histology. Oliguria and high
serum creatinine are due to functional impairment; since
there is no sufficient blood reaching the kidney to be
cleared of these toxins.
Combination of hypotension, hypovolaemia resulting in
diminished renal perfusion is the most common cause of
acute renal failure in hospitalized patients.
When renal hypoperfusion (due to hypotension and/or
hypovolaemia) is not severe enough to cause renal
tubular damage, it will manifest as pre-renal failure in
the form of oliguria and a rise in serum creatinine and
blood urea. Since there is no structural renal damage,
early diagnosis and correction of renal hypoperfusion
results in immediate diuresis and rapid drop in serum
creatinine and blood urea levels.
If hypoperfusion is severe or neglected, renal
compensatory mechanisms will fail and acute tubular
necrosis occurs. In this new situation, correction of
hypoperfusion will not be followed by diuresis or drop
in serum creatinine. Few days or weeks (mean 2-3
weeks) are needed for tubular regeneration and
recovery of kidney function to occur.
II.Acute Intrinsic Renal injury
This includes acute tubular necrosis
(ATN), acute interstitial nephritis and
acute glomerulonephritis.
At this presentation we well discuss ATN
as the other entity will be discussed
separately in other lectures.
Acute Tubular Necrosis
Acute tubular necrosis can be induced
by :
renal hypoperfusion (ischemia).
exposure to nephrotoxins (exogenous
or endogenous toxins).
and frequently by a combination of
both.
Causes of Ischaemic ATN:
A- Blood Loss
Haemorrhage (post partum, surgical or gastrointestinal).
Major trauma
B- Fluid Loss
Gastrointestinal (vomiting or diarrhoea)
Renal (aggressive diuresis or polyuria)
C- Third Space
Haematoma
Illius
Peritonitis
D- Severe vasodilatation as in septicaemia, rapid oedema
formation, liver cell failure.
E- Renovascular disease
Renal artery occlusion by stenosis, embolism or
compression.
Renal vein thrombosis or compression.
Causes of Toxic ATN

(A) Exogenous nephrotoxins include:

Antibiotics: Aminoglycosides ,Amphotericin
,Cephalosporin, Acyclovir, Sulfonamide, Tetracyclines
Bacitracin.
Anaesthetic agents: Methoxy fluorane
Contrast Media:
Analgesics:
Metals: as Mercury, lead, arsenic, bismuth, cadmium,
antimony,
organic solvents: Glycols
Poisons: snake bite, stings, bacterial toxins.
Causes of Toxic ATN

(B) Endogenous nephrotoxins

include
Pigments: Crystals:
Myoglobin Uric acid
Hemoglobin Calcium
Methemoglobin Oxalate
Post renal injury
In post-renal failure, the obstruction of the
urinary tract results in increasing the pressure
above the level of the obstruction up to the
nephron including the urinary space of the
renal glomeruli. When this back pressure
exceeds that of the filtration pressure in the
renal glomeruli, the process of urine
formation will stop with progressive
accumulation of wastes and increase of
serum creatinine and blood urea.
Clinical features of AKI:
1- Usually, the patient gives history of the etiologic
cause such as trauma, shock, haemolysis, drug
intake, infection, or stone disease.

2- Patient may notice a change in urine volume and

character, oliguria is common, but in 10-50% of
cases urine volume will be normal or even higher
(as in toxic ATN) this is called polyuric ATN.
Absolute anuria is highly suggestive of obstructive
ARF (post-renal) or very severe form of ATN
(cortical necrosis).
3- Manifestation of salt and water retention (oedema,
puffiness, hypertension and even heart failure).

4- By time, manifestations of uraemia appear as acidotic

breathing, dyspnea, nausea, vomiting, headache, muscle
twitches and even frank encephalopathy and coma.

5- Patient may present as well with any of the following

complications:
 Complications Of AKI:
Cardiovascular
pulmonary odema arrhythmias
hypertension pericardial effusion
myocardial infarction pulmonary embolism
Metabolic
hyponatremia hyperkalemia
acidosis hypocalcemia
hyperphosphatemia
Neurologic:
coma seizures
Gastrointestinal:
gastritis gastroduodenal ulcers
Haematologic:
anaemia hemorrhagic diathesis
Infections
pneumonia septicemia
UTI
Investigations of AKI:
A-Urinary indices:-
May be helpful in the differentiation
between pre-renal failure and acute
tubular necrosis. Diuretics should not be
given at least during the preceeding 48
hours for these parameters to be valid.
B- Urinary sediment:
Centrifugation of fresh urine sample and examination
of the urinary
sediment may be helpful in diagnosing different causes
of ARF

C- Renal Imaging

D-Renal bx.
TREATMENT OF AKI:
A- Treatment of the cause e.g. any condition
causing renal hypoperfusion, exposure to
toxic drug or chemical or systemic disease.
B- Prevention of AKI:
The timing of intervention to prevent ATN is
important. Protective agents must be
administered at the time of, or immediately
following potential renal insult. This
intervention may prevent or at least blunt the
severity of ATN.
The intervention could be through the following
approaches. In different combinations according
to the clinical situation:
Volume expansion by saline loading.
Diuretic as mannitol and furosemide.
Calcium channel blockers as verapamil and
nifedipine.
Vasodilating agents as dopamine in renal dose
1-2 ug/kg/min
ATP-magnesium chloride.
In case of contrast media, the following additional
points should be adopted, these are:-

Avoid unnecessary contrast procedures.

Avoid multiple contrast exposure within a few
days.
Avoid contrast exposure in high risk patient.
Use the smallest dose possible.
Use of non-ionic contrast is to somewhat safer.
In high risk patient with renal impairment we
can manage to wash the contrast out immediately
after the technique (e.g. coronary angiography)
by haemodialysis.
CHRONIC KIDNEY DISEASE
What is CKD?
Presence of markers of kidney damage for three
months, as defined by structural or functional
abnormalities of the kidney with or without decreased
GFR, manifest by either pathological abnormalities or
other markers of kidney damage, including
abnormalities in the composition of blood or urine, or
abnormalities in imaging tests.

The presence of GFR <60 mL/min/1.73 m2 for three

months, with or without other signs of kidney
damage as described above.
Epidemiology
19 million Americans have CKD
Approx 435,000 have ESRD/HD

Annual mortality rate for ESRD: 24%

CAUSE OF CKD:
The most common causes of CKD are DM,HTN
and glomerulonephritis. Together, these cause
approximately 75% of all adult cases
Diabetes. It causes about 35% of all chronic kidney
disease. High blood sugar levels caused
by DM damage blood vessels in the kidneys. If the
blood sugar level remains high, this damage
gradually reduces the function of the kidneys.
hypertension. It causes another 30% of
all kidney disease. Because HTN often rises with
chronic kidney disease, high blood pressure may
further damage kidney function even when another
medical condition initially caused the disease.
Other etiologies
Renovascular disease
Nephrotic syndrome
Hypercalcemia
Multiple myeloma
Chronic UTI
Signs & Symptoms
General GI
Fatigue & malaise Anorexia
Edema Nausea/vomiting
Ophthalmologic Skin
AV nicking Pruritis
Cardiac Pallor
HTN Neurological
Heart failure MS changes
Pericarditis Seizures
CAD
GFR Calculations
Cockcroft-Gault
Men: CrCl (mL/min) = (140 - age) x wt (kg)
SCr x 0.81

Women: multiply by 0.85

MDRD: USUALLY WE USE COMPUTARISED

FORMULA TO CALCULAT IT :
GFR (mL/min per 1.73 m2) = 186 x (SCr x
0.0113)-1.154 x (age)-0.203 x (0.742 if female) x
(1.12 if African-American)
 Stages of CKD
Stage 1*: GFR >= 90 mL/min/1.73 m2
Normal or elevated GFR

Stage 2*: GFR 60-89 (mild)

Stage 3: GFR 30-59 (moderate)

Stage 4: GFR 15-29 (severe; pre-HD)

Stage 5: GFR < 15 (kidney failure)

Management
Identify and treat factors associated
with progression of CKD
HTN
Proteinuria
Glucose control
Hypertension
Target BP
<130/80 mm Hg
<125/75 mm Hg
pts with proteinuria (> 1 g/d)

Consider several anti-HTN medications with

different mechanisms of activity
ACEs/ARBs
Diuretics
CCBs
HCTZ (less effective when GFR < 20)
Proteinuria
Single best predictor of disease progression

Normal albumin excretion

<30 mg/24 hours
Microalbuminuria
20-200 g/min or 30-300 mg/24 hours
Macroalbuminuria
>300 mg/24 hours
Nephrotic range proteinuria
>3 g/24 hours
Metabolic changes with CKD
Hemoglobin/hematocrit
Bicarbonate
Calcium
Phosphate
PTH
Triglycerides
Metabolic changes
Monitor and treat biochemical
abnormalities
Anemia
Metabolic acidosis
Mineral metabolism
Dyslipidemia
Nutrition
Anemia
Common in CKD
HD pts have increased rates of:
Hospital admission
CAD/LVH
Reduced quality of life
Managing anemia Can improve energy
levels, sleep, cognitive function, and
quality of life in HD pts
Metabolic acidosis
Muscle catabolism

Metabolic bone disease

Sodium bicarbonate
Maintain serum bicarbonate > 22 meq/L
0.5-1.0 meq/kg per day
Watch for sodium loading
Volume expansion
HTN
Mineral metabolism
Calcium and phosphate metabolism
abnormalities associated with:
Renal osteodystrophy
Calciphylaxis and vascular calcification

14 of 16 ESRD/HD pts (20-30 yrs) had

calcification on CT scan
3 of 60 in the control group
Dyslipidemia
Abnormalities in the lipid profile
Triglycerides
Total cholesterol
NCEP recommends reducing lipid levels
in high-risk populations
Targets for lipid-lowering therapy
considered the same as those for the
secondary prevention of CV disease
Nutrition
Think about uremia
Catabolic state
Anorexia
Decreased protein intake
CV disease
70% of HD patients have concomitant
CV disease

Heart disease leading cause of death in

HD patients

LVH can be a risk factor

Evaluation for CKD
Blood Urine
CBC with diff Urinalysis with
SMA-7 with Ca2+ microscopy
and phosphorous Spot urine for
PTH microalbumin
HBA1c 24-urine collection
LFTs and FLP for protein and
creatinine
Uric acid and Fe2+
studies
Ultrasound
 Key points
The serum creatinine level is not
enough!
Target BP for CKD
<130/80 mm Hg
<125/75 mm Hg in proteinuria
HTN and proteinuria are the two most
important modifiable risk factors for
progressive CKD
sekian

ALHAMDULILLAH
HATUR NUHUN